HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Konishi, T Search for Related Content PubMed PubMed Citation Articles by Konishi, T

Department of Neurology, Utano National Hospital, Kyoto, Japan.

1. Ionic currents in Schwann cells cultured from enzymatically dissociated sciatic nerves of newborn mice were recorded by the whole-cell variation of the patch-clamp technique. 2. In these cells only the voltage-dependent K+ currents were recorded. The K+ current was suppressed by quinine, 4-aminopyridine (4-AP) or tetraethylammonium (TEA), their half-suppression concentrations being 22 microM, 0.3 mM and 15 mM, respectively. 3. The peak amplitudes and density of the K+ currents in these Schwann cells increased rapidly during the first 2 days of the culture. 4. In an investigation of the linkage between K+ channels and Schwann cell proliferation, three different K+ channel blockers (quinine, 4-AP and TEA) were added to the medium at different stages of the culture. In media containing sublethal doses of quinine or 4-AP, the start of cell proliferation was delayed when these drugs were added at 12 h or on day 3. The same doses of these drugs applied on day 6, when the Schwann cells were proliferating, did not affect cell proliferation. TEA showed a discrepancy between the dose-dependent blocking of K+ channels and cell proliferation because of its additional cytotoxic effects. 5. It is concluded that voltage-dependent K+ channels in mouse Schwann cells are similar to those observed in human and murine T lymphocytes. These K+ channels are suggested to be involved in Schwann cell proliferation at early stages of development.

This article has been cited by other articles:

				Y. Xu, N. Chiamvimonvat, A. E. Vazquez, S. Akunuru, N. Ratner, and E. N. Yamoah Gene-Targeted Deletion of Neurofibromin Enhances the Expression of a Transient Outward K+ Current in Schwann Cells: A Protein Kinase A-Mediated Mechanism J. Neurosci., November 1, 2002; 22(21): 9194 - 9202. [Abstract] [Full Text] [PDF]

				M. Takahira, N. Sakurada, Y. Segawa, and Y. Shirao Two Types of K+ Currents Modulated by Arachidonic Acid in Bovine Corneal Epithelial Cells Invest. Ophthalmol. Vis. Sci., July 1, 2001; 42(8): 1847 - 1854. [Abstract] [Full Text] [PDF]

				A. Sobko, A. Peretz, O. Shirihai, S. Etkin, V. Cherepanova, D. Dagan, and B. Attali Heteromultimeric Delayed-Rectifier K+ Channels in Schwann Cells: Developmental Expression and Role in Cell Proliferation J. Neurosci., December 15, 1998; 18(24): 10398 - 10408. [Abstract] [Full Text] [PDF]